Dislocation multi-junctions and strain hardening

At the microscopic scale, the strength of a crystal derives from the motion, multiplication and interaction of distinctive line defects called dislocations. First proposed theoretically in 1934 (refs 1-3) to explain low magnitudes of crystal strength observed experimentally, the existence of dislocations was confirmed two decades later. Much of the research in dislocation physics has since focused on dislocation interactions and their role in strain hardening, a common phenomenon in which continued deformation increases a crystal's strength. The existing theory relates strain hardening to pair-wise dislocation reactions in which two intersecting dislocations form junctions that tie the dislocations together. Here we report that interactions among three dislocations result in the formation of unusual elements of dislocation network topology, termed 'multi-junctions'. We first predict the existence of multi-junctions using dislocation dynamics and atomistic simulations and then confirm their existence by transmission electron microscopy experiments in single-crystal molybdenum. In large-scale dislocation dynamics simulations, multi-junctions present very strong, nearly indestructible, obstacles to dislocation motion and furnish new sources for dislocation multiplication, thereby playing an essential role in the evolution of dislocation microstructure and strength of deforming crystals. Simulation analyses conclude that multi-junctions are responsible for the strong orientation dependence of strain hardening in body-centred cubic crystals.     

100-metre-diameter moonlets in Saturn's A ring from observations of 'propeller' structures

Saturn's main rings are composed predominantly of water-ice particles ranging between about 1 centimetre and 10 metres in radius. Above this size range, the number of particles drops sharply, according to the interpretation of spacecraft and stellar occultations. Other than the gap moons Pan and Daphnis (the provisional name of S/2005 S1), which have sizes of several kilometres, no individual bodies in the rings have been directly observed, and the population of ring particles larger than ten metres has been essentially unknown. Here we report the observation of four longitudinal double-streaks in an otherwise bland part of the mid-A ring. We infer that these 'propeller'-shaped perturbations arise from the effects of embedded moonlets approximately 40 to 120 m in diameter. Direct observation of this phenomenon validates models of proto-planetary disks in which similar processes are posited. A population of moonlets, as implied by the size distribution that we find, could help explain gaps in the more tenuous regions of the Cassini division and the C ring. The existence of such large embedded moonlets is most naturally compatible with a ring originating in the break-up of a larger body, but accretion from a circumplanetary disk is also plausible if subsequent growth onto large particles occurs after the primary accretion phase has concluded.     

Deregulation of a Ca2+/calmodulin-dependent kinase leads to spontaneous nodule development

Induced development of a new plant organ in response to rhizobia is the most prominent manifestation of legume root-nodule symbiosis with nitrogen-fixing bacteria. Here we show that the complex root-nodule organogenic programme can be genetically deregulated to trigger de novo nodule formation in the absence of rhizobia or exogenous rhizobial signals. In an ethylmethane sulphonate-induced snf1 (spontaneous nodule formation) mutant of Lotus japonicus, a single amino-acid replacement in a Ca2+/calmodulin-dependent protein kinase (CCaMK) is sufficient to turn fully differentiated root cortical cells into meristematic founder cells of root nodule primordia. These spontaneous nodules are genuine nodules with an ontogeny similar to that of rhizobial-induced root nodules, corroborating previous physiological studies. Using two receptor-deficient genetic backgrounds we provide evidence for a developmentally integrated spontaneous nodulation process that is independent of lipochitin-oligosaccharide signal perception and oscillations in Ca2+ second messenger levels. Our results reveal a key regulatory position of CCaMK upstream of all components required for cell-cycle activation, and a phenotypically divergent series of mutant alleles demonstrates positive and negative regulation of the process.